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NSG 470 > Assessment and mgmt of pt with liver disorders > Flashcards

Assessment and mgmt of pt with liver disorders Flashcards

1
Q

Liver A+P

A
  • Largest gland in the body
  • RUQ (If there is pain in this quadrant it’s probably liver or gallbladder related)
  • Very vascular
  • Receives blood from nutrient rich blood from GI tract via the portal vein
  • Oxygen rich blood from the hepatic artery
  • Mix of oxy and deoxy blood with the hepatocytes
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2
Q

Biliary system

A
  1. Liver produces bile
  2. Bile moves into the bile ducts
  3. Bile moves into the gallbladder for storage or is immediately used
  4. Bile is them moved to the sphincter of oddi
  5. Bile is then excreted into the intestine for fat digestion

Obstruction can lead to N+V and overall sickness

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3
Q

Functions of the liver: Glucose

A

Metabolism and regulation of glucose serum concentration

q

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4
Q

Functions of the liver: Ammonia

A

Converts it into urea
-In liver disease, it prevents the conversion, increasing ammonia levels. Which can be detrimental

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5
Q

Functions of the liver: Protein metabolism

A
  • Formation of albumin, globulins, clotting factors, lipoproteins
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6
Q

What is required for the synthesis of prothrombin and other clotting factors

A

Vitamin K

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7
Q

Functions of the liver: Vitamin and iron storage

A

ABD

A/D are Fat soluble vitamins

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8
Q

Functions of the liver: Bile formation

A
  • Water,
  • Electrolytes
  • bicarb
  • lecithin
  • fatty acids
  • cholesterol
  • bilirubin
  • bile salts
    *
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9
Q

Functions of the liver: Bilirubin excretion

A

To the gallbladder and intestine

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10
Q

Functions of the liver: Drug metabolism

A

Metabolizes drugs
First pass effect

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11
Q

First pass effect

A

Liver almost completely metabolizes a drug the first time it sees it and requires a higher dose for its therapeutic level

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12
Q

Important labs related to the liver

A

Aminotransferases
* AST
* ALT
* GGT
* LDH
Protein and albumin
Bilirubin
Clotting factors
* PT/INR
* Plt
Ammonia
Lipids

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13
Q

AST> ALT

A

Myocardial necrosis

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14
Q

ALT> AST

A

Liver issues

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15
Q

Normal AST

A

8-48 U/L

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16
Q

Normal ALT

A

7-55 U/L

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17
Q

Normal ALP

A

45-115 U/L

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18
Q

Normal bilirubin

A

0.1-1.2 mg/L

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19
Q

Normal Total protein

A

6.3-7.9 mg/L

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20
Q

Normal albumin

A

3.5-5 ml/L

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21
Q

Transaminases

A

ALT, AST and GTT
Indicators of injury to liver cells, useful in detecting hepatitis

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22
Q

Alanine aminotransferase (ALT)

A

Increased primarily in liver disorders used to monitor the course of hepatitis, cirrosis and the effectiveness of treatments that may be toxic to the liver

Main one

Transaminase

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23
Q

Aspartate aminotransferase (AST)

A

Not specific to liver diseases may be increased in cirrhosis, hepatitis, and liver cancer

Will be elevated but not to the degree of ALT

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24
Q

Gamma-glutamyl transferase (GTT)

A

Associated with cholestasis (Blocked bile), alcoholic liver disease

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25
Q

Diagnostics for liver dysfunction

A
  • Ultrasound
  • CT scan
  • MRI
  • ERCP (Endoscopic retrograde cholangiopancreatography)
  • Transient liver elastography (Stiffness of the liver)
  • Liver biopsy (Invasive)
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26
Q

Health history liver dysfunction

A
  • Exposure to hepatotoxic substances (Environmental exposures)
  • Infections (Hepatitis)
  • Travel, substance use disorder
  • Lifestyle (High risk behaviors)
  • Meds, OTC supplements (Patient won’t tell you all the supplements that they take)
  • Familial liver disorders
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27
Q

Physical assessment with liver dysfunction: Skin

A
  • May be pale from anemia
  • Jaundice
  • Jaundice can lead to pruritus and excoriations
  • Peticuli
  • Spider angiomas
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28
Q

Physical assessment with liver dysfunction

A
  • Skin
  • Cognitive status
  • Motor function
  • Abdomen: Palpation and percussion
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29
Q

Manifestations of liver disease

A
  • Cognitive changes
  • Altered sleep wake
  • Gastroesophageal bleeding- hematemesis, melena
  • Splenomegaly
  • Ascites
  • Jaundice
  • Petechiae, ecchymosis, nosebleeds
  • Palmar erythema
  • Spider angiomas
  • Dependent peripheral edema of extremities and sacrum
  • Asterixis
  • Fetor hepaticus
  • Gyneo, testicular shrinkage
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30
Q

Asterixis

A

Coarse tremor that causes a flapping motion of the wrist to occur

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31
Q

Fetor hepaticus

A

Breath smells fruity, or stool

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32
Q

Why does gyno and testicular shrinkage occur in liver disease

A

Liver cant break down estrogen leading to increased levels

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33
Q

RUQ pain

A

Inflammation of the liver, when liver disease progresses and cirrhosis occurs, the liver will shrink down and pain will subside

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34
Q

Modified Child-Pugh Classification: One point assigned

Probably dont need to know

A
  1. Ascites: Absent
  2. Bilirubin: < 2
  3. Albumin: >3.5
  4. Prothrombin time: 1-3
  5. Encephalopathy: None

Probably dont need to know

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35
Q

Modified Child-Pugh Classification: Two points

Probably dont need to know

A
  1. Ascites: Slight
  2. Bilirubin: 2-3
  3. Albumin: 2.8-3.5
  4. Prothrombin time: 4-6
  5. Encephalopathy: Grade 1-2

Probably dont need to know

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36
Q

Modified Child-Pugh Classification: Three points

Probably dont need to know

A
  1. Ascites: Moderate
  2. Bilirubin: > 3
  3. Albumin: < 2.8
  4. Prothrombin time: >6
  5. Encephalopathy: Grade 3-4

Probably dont need to know

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37
Q

Hepatic dysfunction Causes

A
  • Fatty liver disease (Non-alcoholic fatty liver disease, Nonalcoholic steatohepatitis)
  • Infection (Hepatitis)
  • Cirrhosis of the liver (Compensated vs decomp)
  • Liver failure (Acute, Endstage)
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38
Q

Complications of hepatic dysfunction

A
  • Jaundice (Billirubin build up)
  • Portal hypertension
  • Varicies (esophgeal)
  • Acities
  • Hepatic encephalopathy and coma
  • Nutritional deficiencies (Often with alc)
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39
Q

Jaundice: Hepatocellular

A
  • Yellow or greenish-yellow sclera and skin (Not too much discoloration)
  • Bilirubin levels greater than 2
  • Most commonly associated with liver disease
  • Dmg liver cells from infection, excessive alc use, and prolonged obstructive jaundice
  • Mild to severely ill
  • Lack of appetite, N+V, weight loss
  • Malaise, fatigue, weakness
  • HA, chills , fever, infection
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40
Q

Jaundice: Obstructive

A
  • Yellow or greenish-yellow sclera and skin
  • Bilirubin levels greater than 2
  • Most commonly associated with liver disease
  • Extrahepatic (Gallstones, inflammatory processes, tumor)
  • Intrahepatic (Stasis, thickening of bile in canaliculi)
  • Dark orange/brown colored urine, Clay colored stool
  • Indigestion and intolerance of fats, impaired digestion
  • Pruritus
  • Skin excoriation from scratching (Jaundice makes you itchy)

More jaundiced than other forms of jaundice

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41
Q

Jaundice: Hemolytic

A
  • Yellow or greenish-yellow sclera and skin
  • Bilirubin levels greater than 2
  • From the breakdown of RBC
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42
Q

Portal hypertension

A
  • Obstructed blood flow through the liver results in increased pressure throughout the portal venous system
  • Causes Ascites
  • Causes Esophageal and gastric varices
  • Splenomegaly sometimes too

(Essentially due to this pressure, it forces fluid to follow the path of least resistance and go where it normally woudnt )

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43
Q

Ascites

A

Caused by portal hypertension
* Decreased serum osmotic pressure with movement of albumin from intravascular space to extravascular space including peritoneal cavity: Peripheral edema and ascites
* Genital swelling
* Can also occur from cancer, Kidney disease and HF

Essentially albumin gets moved into peritoneal space and water follows it

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44
Q

Assessment of ascites: Measurement

A
  • Record the abdominal girth and weight daily (Can have rapid weight gain and fluid buildup)
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45
Q

Assessment of ascites: Abdomen

A
  • Striae
  • Distended veins (Caput medusae)
  • Abdominal hernia
46
Q

Assessment of ascites: Assessment for fluid

A
  • percussion for a shifting dullness (Dullness=fluid)
  • Fluid wave
47
Q

Assessment of ascites: Dyspnea

A

Dyspnea can occur with ascites for 3 main reasons
1. Anemia
2. Fluid is pressing on the diaphragm, limiting expansion
3. Fluid has moved into the pleural cavity, causing a pleural effusion

48
Q

Assessment of ascites: Electrolytes

A

Monitor for potential fluid and electrolyte imbalances
* Sodium: Reabsorbed by the kidney
* Potassium is often imbalanced
* Renal function

49
Q

Fluid wave test

A

Test for ascites
* Pt puts hand midline and then the nurse presses on one side, if fluid is in the abdomen you are able to feel it on the opposite side, if not its not fluid

50
Q

Dullness

A

Fluid, and it should shift with gravity with ascites

51
Q

Mgmt of ascites

A
  • Low sodium, fluid restrictions ( People hate this)
  • Diuretics (Spironolactone is the choice, also furosemide)
  • Bedrest (During exasperations, standing up causes fluid retention, as ADH levels increase, bed rest helps ya pee)
  • Paracentesis (Draining the abdomen, can cause hypotension)
  • Administration of salt poor albumin
  • Transjugular intrahepatic portosystemic shunt (TIPS) (Shunt to help with portal hypertension)
  • Peritoneal drains
52
Q

What med is used with ascites and why

A

Spironolactone: First line therapy due to its K+ sparing effects

53
Q

Spironolactone

A

K+ sparing diuretic
Blocks the activity of aldosterone, increasing urination and sodium excretion
Decreased overall fluid volume

Can be given with furosemide to decrease K+ levels

54
Q

Spironolactone: Side effects

A
  • Mild
    Hyponatremia, Hypomagnesemia, hypocalcemia, abdominal pain, N+V, leg cramping, dizziness, lightheadedness, male gyno
  • Serious
    Hyperkalemia, hypotension , decreased kidney function, anaphylaxis, steven johnson syndrome, toxic epidermal necrolysis
55
Q

Esophageal varices

A
  • Occurs as liver disease progresses
  • Dilated, knotty veins of esophagus and stomach that develop due to portal vein hypertension and obstruction of portal venous circulation
  • Manifestations: GI bleeding hematemesis, melena and hemorrhagic shock
  • Prevention: Pt with cirrhosis should undergo screening endoscopy every 2-3 years to monitor for varices

GI bleeding is main thing, they are vomiting alot of blood

56
Q

mgmt of esophageal varices

A
  • Balloon tamponade (Needs sedation), saline lavage (Cold water on the bleeding wound)
  • ICU most likely
  • Treat hemorrhagic shock (ABC)
  • Oxygen, maintain Airway may need intubation
  • IV fluids, electrolytes, volume expanders and blood products
  • Vasopressin, Somatostatin, Octreotide
  • Nitro in combo with vasopressin to reduce coronary vasoconstriction
  • Propranolol and nadolol (Beta blockers), decreasing portal pressure
57
Q

Surgical mgmt of varices

A
  • Endoscopic sclerotherapy
  • Endoscopic variceal ligation (Esophageal banding, placing a band to stop blood flow to that area)
  • Transjugular intrahepatic portosystemic shunt (TIPS)
  • Surg mgmt
58
Q

Hepatic Encephalopathy (HE) and coma

A
  • Life threatening issue
  • Two main issues: HE and coma
    1. Hepatic insufficiency
    2. Portosystemic shunting
  • Accumulation of ammonia levels in the blood (Ammonia enters the brain and causes neuro changes)
  • Early signs: Mental status changes and motor disturbances
59
Q

Hepatic insufficency

A

Cause of Hepatic Encephalopathy and coma
inability for the liver to detox toxic by products of the metabolism (ammonia)

60
Q

Portosystemic shunting

A

Cause of Hepatic Encephalopathy and coma
Collateral vessels develop allowing elements of the portal blood (Filled with toxins extracted by the liver) to enter they systemic circulation

61
Q

Assessment and Stages of Encephalopathy

A

Assessment
* EEG
* Changes in LOC and motor function (First sign)
* Potential seizures
* Fetor hepaticus (Poop breath) asterixis (Flappy wrist)
* Monitor fluid, electrolyte and ammonia levels
Stages
* 1-4

62
Q

Stages of Encephalopathy: Stage 1

A
  • Normal LOC with periods of lethargy and euphoria
  • Reversal of day night sleep patterns
  • Impaired writing and ability to draw line figures
  • Normal EEG
63
Q

Stages of Encephalopathy Stage 2

A
  • Increased drowsiness
  • Disorientation
  • Inappropriate behavior
  • Mood swings
  • Agitation
  • Asterixis
  • Fetor hepaticus
  • Abnormal EEG with generalized slowing
64
Q

Stages of Encephalopathy: Stage 3

A
  • Stupor: Difficult to rouse
  • Marked confusion
  • Incoherent speech
  • Asterixis
  • Absent deep tendon reflexes
  • Rigidity of extremities
  • EEG markedly abnormal
65
Q

Stages of Encephalopathy: Stage 4

A
  • Comatose, may not respond to painful stimuli
  • Absence of asterixis
  • Absence of deep tendon reflexes
  • Flaccidity of extremities
  • EEG markedly abnormal
66
Q

Mgmt of Hepatic Encephalopathy

A
  • Reduce protein intake
  • Reduction of ammonia from systemic circulation by gastric suction, lactulose, enemas, oral antibiotics (Kill ammonia producing bacteria in gut)
  • Discontinue sedatives, analgesics and tranquilizers and any other med which can affect liver function
67
Q

Fatty liver disease

A
  • Lipids accumulate in hepatocytes
  • NAFLD
  • NASH
  • Combination of obesity and heavy drinking -> severe liver dmg (Can take 20-30 yrs to develop into ESRD)
  • Those at risk should be monitored closely for S+S liver dysfunction

Obesity and drinking

68
Q

Fatty liver disease

A
  • Lipids accumulate in hepatocytes
  • NAFLD
  • NASH
  • Combination of obesity and heavy drinking -> severe liver dmg (Can take 20-30 yrs to develop into ESRD)
  • Those at risk should be monitored closely for S+S liver dysfunction

Obesity and drinking

69
Q

Non-alcoholic fatty liver disease (NAFLD)

A

Less serious than NASH
Associated with obesity

70
Q

Non-alcoholic steatohepatitis

A

More serious than NAFLD
Results in dmg, fibrotic changes in the liver (Cirrhosis)

Assosiated with obesity

71
Q

Viral hepatitis

A
  • ABCDEG
  • Causes necrosis and inflammation of liver cells, resulting in liver enlargement and obstruction of blood flow to the liver
72
Q

Non-viral hepatitis

A
  • Toxic and drug induced
  • Alc, hepatotoxic chemicals, Botanical agents
  • S+S: Anorexia, N+V, jaundice, hepatomegaly, bleeding, chills, fever, rash, pruritus
  • Recovery unlikely of prolonged period, with exposure and symptoms

Acetaminophen, mushrooms, carbon tetracholoride

73
Q

Fecal oral hepatitis

A

A/ E

74
Q

Common findings in hepatitis

A
  • Flu like symptoms (Fatigue, Decreased appetite, N, Ab pain, joint pain)
  • Physical (Fever, vomiting, dark colored urine, clay colored stool, jaundice)
75
Q

Types of hepatitis: Type A

General info

A
  • Source: Feces
  • Route of transmission: Fecal oral
  • Chronic infection: No
  • Prevention: Pre and post immunizations
76
Q

Types of hepatitis: Type B

General info

A
  • Source: Blood, blood derived bodily fluids
  • Route of transmission: Percutaneous membranes
  • Chronic infection: Yes
  • Prevention: Immunization
77
Q

Types of hepatitis: Type C

General info

A
  • Source: Blood, Blood derived body fluids
  • Route of transmission: Percutaneous permucosal
  • Chronic infection: Yes
  • Prevention: Blood donor screening , risk behavior modification
78
Q

Types of hepatitis: Type D

General info

A
  • Source: Blood/ blood derived body fluids
  • Route of transmission: Percutaneous permucosal
  • Chronic infection: Yes
  • Prevention: Immunizations, risk behavior modification

Cant have D without B

79
Q

Types of hepatitis: Type E

General info

A
  • Source: Feces
  • Route of transmission: Fecal oral
  • Chronic infection: No
  • Prevention: Ensure safe drinking water
80
Q

Hepatitis A: HAV

A
  • Spread by poor hand hygiene or sanitation **Fecal oral **
  • Ingestion of contaminated food or water, especially shellfish
  • Contact with infected stool (Incontinence, anal sex)
  • Hep A antibodies reveal presence of Hep A
  • S+S: Mild flu like symptoms, low grade fever, anorexia, later jaundice , and dark urine , indigestion and epigastric distress enlargement of liver and spleen
  • Mgmt: Bedrest during acute stage, and supportive care

Not chronic

81
Q

Hepatitis A: HAV

A
  • Spread by poor hand hygiene or sanitation **Fecal oral **
  • Ingestion of contaminated food or water, especially shellfish
  • Occurs often with food service industry
  • Contact with infected stool (Incontinence, anal sex)
  • Hep A antibodies reveal presence of Hep A
  • S+S: Mild flu like symptoms, low grade fever, anorexia, later jaundice , and dark urine , indigestion and epigastric distress enlargement of liver and spleen
  • Mgmt: Bedrest during acute stage, and supportive care

Not chronic

82
Q

Prevention and mgmt of hep A

A
  • Hep A immunization
  • Immune globulin for passive immunity to close contacts, non-immune and institutionalized
  • Good handwashing, safe water and proper sewage disposal
  • No treatment except supportive
83
Q

Hep B: HBV

A
  • Transmitted via: Blood, saliva, semen , and vaginal secretions, STI, transmitted to infant at birth
  • Major cause of cirrhosis and liver cancer (Chronic infections)
  • Manifestations: Insidious and variable, similar to hep , loss of appetite, dyspepsia, ab pain , aching, malise and weakness, +/- jaundice (Clay colored stool, dark urine
  • Hep B antigen indicates a person is infectious, chronic carriers are infectious
  • Can be chronic
84
Q

Mgmt of hep B

A
  • Acute infection: no meds, supportive care
  • Chronic infection: They are unable to clear the virus and given antivirals are needed
  • Bedrest and nutritional support
  • Passive immunization with hep B immune globulin
  • Vaccine is available
85
Q

Hep C: HCV

A
  • Transmission is via blood
  • 1/3 cases of liver cancer are caused by this and is the #1 reason for liver transplant
  • Risk factors are the same for Hep B, Blood and all that
  • Symptoms are usually mild if at all
  • Can have the disease and not know they have it, leading to transmission to others
  • Chronic cases are common
86
Q

Mgmt of Hep C

A
  • No found benifit to rest, vitamins and diet
  • Give Direct acting antivirals, can be undetectable and cured 8-12 weeks of completed treatment
  • Alc progresses diseases, pt cannot drink when they have hep C
  • Meds that affect the liver should be avoided
87
Q

Direct acting antivirals

A
  • Newer med that is given for hep C
  • Destroys the virus directly, preventing further replication
  • More effective than prior antivirals, less side effects
  • Can be undetectable and cured in 8-12 weeks

Simeprevir, sofosbtavit, paritaprevir, glecaprevir, grazoprevir

88
Q

Hep D: HDV

A
  • Main thing is you cant have Hep D without B (Needs the hep B antigen)
  • Blood and sexual contact transmission, injectable drugs, hemodialysis and recipients of multiple blood transmission
  • S+S similar to hep B, but more likely to develop acute, fulminant liver failure or chronic active hepatitis and cirrhosis
  • High dose interferon For ONE year
89
Q

Hep E: HEV

A

Fecal oral transmission, contaminated water mainly
* Resembles hep A, self limiting, abrupt onset, not chronic
* No treatment except supportive care

90
Q

T/F only persons with Hep A can get Hep E

A

False, only pt with hep B can get hep D

91
Q

Alcoholic Cirrhosis

A

Scar tissue surrounds the portal areas, most common

92
Q

Post necrotic Cirrhosis

A

Broad bands of scar tissue across the liver

93
Q

Biliary cirrhosis

A

Scarring occurs in the liver around the bile ducts
Occurs from chronic biliary obstruction

94
Q

Hepatic Cirrhosis: Patho

A

Replacement of normal liver tissue with diffuse fibrosis
Liver becomes fibrotic and nodular

95
Q

Manifestations of hepatic cirrhosis

A
  • Liver enlargement (Shrinking later into the disease, when fibrosis progresses)
  • Portal obstruction
  • Ascites
  • Infection/peritonitis
  • Varices
  • Edema
  • Vitamin deficiency
  • Anemia
  • Mental deterioration
96
Q

Common drugs that are assosiated with liver failure

Probably dont need to know

A
  • Acetaminophen
  • Alc
  • Coke
  • Nsaids
  • Kava Kava
  • Mushrooms
97
Q

Liver transplant success

A

Depends on successful Immune suppression

98
Q

What is used to allocate cadaver livers

A

MELD score

99
Q

Graft vs host disease

A
  • Rejection of transplanted liver
  • S+S of acute liver injury like inflammation of liver
100
Q

Liver transplant criteria

A
  • Stringent criteria if they have primary liver cancer, small early lesions (1 x < 5 cm or 3 x < 3 cm)
  • End stage liver disease: whole liver from deceased donor or partial liver from live donor
101
Q

What lobe of the liver is donated in a live liver transplant

A

Right

102
Q

Immunosuppressants given for liver transplant

A
  • Cyclosporine
  • Tacrolimus
  • Sirolimus
  • Everolimus
  • Mycophenolate

Corticosteroids are only given when neeeded, (Induction or rejection)

103
Q

Immunosuppressants given for liver transplant

A
  • Cyclosporine
  • Tacrolimus
  • Sirolimus
  • Everolimus
  • Mycophenolate

Corticosteroids are only given when neeeded, (Induction or rejection)

104
Q

Where is jaundice first seen

A

Sclera of the eye

105
Q

Education for viral hep

A
  • Contact precautions
  • Educate pt and fam about preventing transmission
  • Avoid sex until hep antigen testing is neg
  • Use proper hand hygiene and contact precautions
  • Refer for substance abuse program
  • Avoid alc and injection drugs
  • Needle syringe exchange programs
106
Q

Liver failure /disease education: Resp care

A
  • Comfort measures by positioning pt to ease resp effort (Can be difficult due to presence of ascites
  • Sit in a chair or elevate HOB 30 degrees with feet elevated (Lay them flat during the acute period)
  • Oxygen, deep breathing and coughing
  • Call for changes in resp status (Can indicate pleural effusion)
107
Q

Liver failure /disease education: Skin integrity

A
  • Measures to prevent pressure injuries (T/P 2 hrs)
  • Reduce pressure points
  • Monitor for skin breakdown (Especially with peripheral edema)
  • Measures to alleviate pruritus (Gentle skin care, avoid soap, washing with cool water, applying lotion to decrease the itching, keep lotion in the fridge
  • Assess for excoriations bruising, petechiae, jaundice
108
Q

Liver failure /disease education: Nutrition

A
  • High carb, high cal, moderate fat/protein and low sodium
  • Vitamin supplements (Thiamine, folate, multivitamins)
  • Small frequent meals
  • Proper positioning during meals
  • Label reading for salt content, don’t add salt to food
109
Q

Liver failure /disease education: Fluid balance

A

Monitor and measure increasing abdominal distension, peripheral edema
Keep I+O daily weights
Restrict fluids if prescribed

110
Q

Liver failure /disease education: Activity

A
  • Bedrest during acute illness
  • Planned exercise and rest periods
111
Q

Liver failure /disease education: Neuro status

A
  • Monitor and call for deteriorating mental status and dementia consistent with hep encephalopathy
  • Monitor for asterixis and fetor hepaticus
  • Lactulose if elevated ammonia level/ hepatic encephalopathy to reduce ammonia
112
Q

Liver failure /disease education: GI status

A
  • If ascites measure abdominal girth daily
  • Observe for potential bleeding, from varices (S+S: Anxiety, restlessness, Tachycardia, N+V, Hematemesis, melena)
  • Pain mgmt: Based on provider, analgesics, antacids acid blockers, antiemetics

NSG 470 (26 decks)

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